89 research outputs found

    Preliminary Report on the Feasibility of Using the IUCF Cooler Ring Synchrotron as an Electron Storage Ring

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    This research was sponsored by the National Science Foundation Grant NSF PHY-931478

    Transitory FGF treatment results in the long-lasting suppression of the proliferative response to repeated FGF stimulation.

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    FGF applied as a single growth factor to quiescent mouse fibroblasts induces a round of DNA replication, however continuous stimulation results in arrest in the G1 phase of the next cell cycle. We hypothesized that FGF stimulation induces the establishment of cell memory, which prevents the proliferative response to repeated or continuous FGF application. When a 2-5 day quiescence period was introduced between primary and repeated FGF treatments, fibroblasts failed to efficiently replicate in response to secondary FGF application. The establishment of “FGF memory” during the first FGF stimulation did not require DNA synthesis, but was dependent on the activity of FGF receptors, MEK, p38 MAPK and NFκB signaling, and protein synthesis. While secondary stimulation resulted in strongly decreased replication rate, we did not observe any attenuation of morphological changes, Erk1/2 phosphorylation and cyclin D1 induction. However, secondary FGF stimulation failed to induce the expression of cyclin A, which is critical for the progression from G1 to S phase. Treatment of cells with a broad range histone deacetylase inhibitor during the primary FGF stimulation rescued the proliferative response to the secondary FGF treatment suggesting that the establishment of “FGF memory” may be based on epigenetic changes. We suggest that “FGF memory” can prevent the hyperplastic response to cell damage and inflammation, which are associated with an enhanced FGF production and secretion. “FGF memory” may present a natural obstacle to the efficient application of recombinant FGFs for the treament of ulcers, ischemias and wounds

    Sources of acoustic emission during fatigue of Ti-6Al-4V: effect of microstructure

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    The fundamentals of acoustic emission (AE) analysis of fatigue cracking were applied to Ti-6Al-4V. The effect of microstructure on the characteristics of the AE events generated and the failure mechanisms which produced AE in Ti-6Al-4V were established. Lamellar microstructures generated one to two orders of magnitude more emission than equiaxed microstructures. The combination of larger grain size, more continuous α/β interfaces, more tortuous crack-front geometry, cleavage and intergranular fracture in lamellar microstructures accounts for the greater amount of emission. For lamellar microstructures, most AE events were generated in the upper 20% of the stress range, whereas in equiaxed microstructures, most events were generated at lower stresses. Most AE events were generated during crack opening and also at low stresses. AE events having high level intensities were also generated at stresses other than the peak stress. This is because in titanium alloys, which have both high strength and toughness, AE events are generated from both plastic zone extension and crack extension.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44721/1/10853_2004_Article_BF00542927.pd

    Excitation of giant resonances in <SUP>92</SUP>Zr by inelastic scattering of 115 MeV protons

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    The differential cross sections for the excitation of giant resonances in 92Zr have been measured in the angular range 14 to 30&#176; by inelastic scattering of 115 MeV protons. The low energy octupole region Ex=5-10.5 MeV can be explained as due to excitation of L=3 and L=4 multipoles. The composition of the differential cross section for the giant resonance region (Ex=10.5-20 MeV) can be described in terms of the percentage energy-weighted sum-rule strength as 63% giant monopole resonance, 65% giant dipole resonance, 48% giant quadrupole resonance, and 20% L=4 resonance
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